Satellite phage P4 and its helper P2 are an excellent model system for the in vitro and in vivo study of viral morphogenesis and structure. Satellite phage P4 depends on all the late gene products of its helper P2 for normal lytic multiplication. P4 uses the P2 helper late gene products to assemble a tail identical to that of its helper. It also "directs" the assembly of a P4 head composed mostly (perhaps completely) of P2 proteins which is one-third the size of the P2 head. We propose to determine whether it is the P4 DNA or a P4 induced size "directing" protein which is responsible for the assembly of P4 size heads. We will use the following approaches: (1) isolation and study of P4 head-size mutants; (2) gel electrophoretic and tryptic peptide analysis of the head proteins of P2 and P4; and (3) study of P2 and P4 head assembly and DNA packaging in vitro. The P2-P4 system is also a promising model system for study of the positive control of gene expression. P4 can transactivate (induce) the 18 late genes of a repressed P2 prophage helper. This transactivation occurs without excision or replication of the prophage genome. The induction of the prophage late genes is so active that over 200 P4 particles are released. We propose to determine how P4 transactivates the P2-prophage helper late genes. We will begin this work by isolating P4 mutants which cannot transactivate P2 late genes. Many animal virus systems are known in which more complicated but analogous satellite-helper relationships exist. Oncogenesis may be caused by latent viruses, defective viruses or by special genes incorporated into a host cell chromosome. Defective animal viruses like P4 might exist as latent oncogenes, while viruses now considered innocuous could serve as helpers for such oncogenic satellite viruses. A review article on the analogy between the P2-P4 interaction and similar phenomena among carcinogenic animal viruses is in press in "Progress in Medical Virology".